THE INFLUENCE OF INTRACARDIAC
BARORECEPTORS ON VENOUS RETURN,
SYSTEMIC VASCULAR VOLUME AND
PERIPHERAL RESISTANCE
John Ross Jr., … , Charles J. Frahm, Eugene Braunwald
J Clin Invest. 1961;40(3):563-572. https://doi.org/10.1172/JCI104284.
Research Article
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http://jci.me/104284/pdf
THE INFLUENCE OF INTRACARDIAC BARORECEPTORS ON VENOUS RETURN, SYSTEMIC VASCULAR VOLUME
AND PERIPHERAL RESISTANCE
By JOHN ROSS, JR., CHARLES J. FRAHM AND EUGENE BRAUNWALD
(Fromn the Section of Cardiology, Clinic of Surgery, National Heart Institute, Bethesda, Md.)
(Submitted for publication August 10, 1960; accepted November 3, 1960)
The presence of baroreceptors in the walls of the cardiac chambers and the pulmonary vascular
bed is now well established, and their function in the reflex control of the circulation has been the
subject of a number of investigations (1-11).
Action potentials have been recorded from af-ferent fibers originating in the heart and lungs
(1, 2), and elevation of pressures within the ven-tricular chambers (3-9) and pulmonary
vascu-lar bed (4, 10, 11) has resulted in bradycardia (3-10), a decline in systemic arterial pressure (4-9, 11), and either apnea (5, 10) or hyperpnea (4, 11). In a previous report from this labora-tory, evidence was presented that the carotid baroreceptors reflexly influence total venous
re-turn and systemic vascular volume (12). The present investigations were undertaken to deter-mine whether or not these hemodynamic param-etersarealso modified by activation of intracardiac baroreceptors. Studies to localize these receptors within the heart were also carried out.
METHODS
Seventeen dogs weighingfrom 15.1 to23.0 kg,average,
17.2, were anesthetized with morphine (2 mg per kg),
chloralose (48 mg per kg), and urethan (480 mg per
kg). Following tracheal intubation, a bilateral thoraco-tomywas performed through the fourth intercostal space and the sternum was transected. Heparin (2 mg per kg) was then administered intravenously. The femoral artery was cannulated, large cannulae were inserted into each vena cava through the right atrium, and total body perfusion was carried out with a pump-oxygenator
sys-tem as described elsewhere (13). Briefly, blood was
drained by gravity from the venae cavae into a rotating
disc oxygenator and was returned to the femoral artery bymeansof aroller pump througha recording rotameter
(14) whichcontinuouslymetered theperfusion rate.
Sys-temicperfusionrates rangedfrom 73to 109 andaveraged
96 ml per kg. Blood temperature was maintained
be-tween 340 and 37° C bymeans of a heating coil around the oxygenator. In 10 dogs, measurements of altera-tions in the volume of blood in the extracorporeal cir-cuit were carried out. Changes in the level of blood in
the oxygenator were detected by means of sensing elec-trodes (15), and blood was added to or removed from
a calibrated reservoir so that the volume of blood in the oxygenator remained constant. Alterations in
extra-corporeal blood volume, which reflected reciprocal changes in the intravascular blood volume, were meas-ured by recording the level in the calibrated reservoir at 1 minute intervals. In 3 animals, intravascular blood was maintained at a constant volume by increasing or decreasing the arterial pump output; with this maneuver the effect of any intervention on venous return could be determined (16). For example, when venous return to the oxygenator diminished, the pump output was de-creased manually at a rate sufficient to maintain the vol-ume of the extracorporeal circuit constant.
Pressures were measured in the aorta and the inferior vena cava through catheters inserted into small branches of the femoral artery and vein; pressures in the right and left ventricles were obtained by means of catheters inserted directly through the ventricular walls, and in the left atrium by means of a catheter introduced through a pulmonary vein. All pressures were measured with Statham pressure transducers and were recorded
con-tinuously, together with the systemic perfusion rate, on a multichannel oscillograph. Since the systemic per-fusion rate was held constant throughout each experi-ment, any change in arterial pressure reflected an iden-tical change in peripheral resistance.
In order to study the reflex effects of changes in in-tracardiac pressure, two types of preparations were em-ployed. In the first preparation, utilized in Dogs 14, 15
and 16 (TableI),the aorta wasoccluded above the
coro-naryarteries, andbloodwas suppliedtothe heartthrough
a line which originated between the pump and the flow-meter. Total systemic perfusion rate was held constant.
In these experiments, blood entered the left ventricle through a cannula which had been inserted through the apex. The rate of blood flow into the heart, which de-termined the pressure in the left side of the heart, was
regulated by means of a screw clamp on the inflow line. This bloodwas pumped by the left ventricle into the
aor-tic segment proximal to the occlusive clamp, thence
through the coronary circulation, and was returned to
the pump oxygenator by means of a large drainage tube placed in theright ventricle via the azygos veina-nd right atrium. Although this preparation was satisfactory for
studying the effects of changes in intracardiac- pressures
on peripheral resistance, it was unsuitable for the meas-urement of alterations of intravascular blood:volume and
JOHN ROSS, JR., CHARLES J. FRAHM AND EUGENE BRAUNWALD
venous return; when the blood flow to the heart was
in-creased, a significant volume was necessarily diverted
from the extracorporeal circuit into the cardiac cham-bers and pulmonary circulation.
Accordingly, in the second preparation, blood was
cir-culated through the heart by utilizing a separate circuit, entirely isolated from the pump-oxygenator system
(Fig-ure 1). Oxygenated blood drained from a reservoir
through a cannulated pulmonary vein and into the left
side of the heart. In addition to the drainage cannula placed in the right ventricle, a tube was inserted into a
segmental pulmonary artery to assure complete
empty-ing of the right heart and pulmonary artery; the blood from these two drainage tubes was collected in an acces-sory reservoir. Circulation through the lungs was
pre-vented by mass ligation of each hilum. Alterations in pressure inthe left side of the heart could be induced by
varying the inflow fromthe reservoir while the ascending
aorta was kept clamped. When the inflow of blood to
the pulmonary vein was increased, left heart pressures rose, since the only egress of blood was through the
coronary bed. Pressure in the right side of the heart
could be modified by varying the resistance in the right ventricular and pulmonary arterial drainage lines, since clamping of the lines resulted in a "damming up" of
blood in the right side of the heart. When left ventricu-lar systolic pressure was maintained at a level exceeding
approximately 70 mm Hg, the heart continued to beat satisfactorily for several hours. During each
experi-ment, control pressures, extracorporeal blood volume
and heart rate were determined for at least 4 minutes,
and following each intervention, measurements were
re-corded continuously for another 4 to 8 minutes. This preparation was employed in 14 dogs, two of which (7
and 8, Table I) had been subjected to splenectomy
sev-eral weeks prior to study.
In an effort to define the activity of the intracardiac
receptors more precisely, bilateral mass ligation of the
carotid bulb was performed in the 3 dogs in which the
first preparation was employed and in 10 of the 14
ex-periments utilizing the second preparation. In 9 of the
10 dogs in the lattergroup, the aortic baroreceptors were
TABLE I
Hemodynamic effects of changes inintracardiacpressures
LV press. LApress. RV press. Ao press. HR
Dog __
Intervention no. Wt A B A B A B A B AB.V. AS.F. A B
kg mmHg cmH20 mmHg mmHg ml mi/min
i+ 19.0 70/6 200/17 8 23 25/3 60/20 66 40 +160 126 120
75/0 210/10 10 22 25/2 75/15 75 50 -220 210/10 65/0 22 10 75/15 20/5 50 69 + 70
2+ 16.6 75/1 220/15 6 14 12/9 85/25 120 90 96 102
3+ 19.0 68/3 190/5 6 20 2/0 60/5 84 60 -540
Left andright 190/5 75/5 20 6 60/5 2/0 60 74 +260
heart pressures 4+ 23.0 77/5 235/22 6 25 1/0 60/10 67 50 -590 120 120
altered 235/30 60/5 25 5 60/10 1/0 58 68 +195 120 132
100/8 225/40 8 40 1/0 60/10 63 52 +110 114 114
5 18.3 73/7 225/20 7 30 1/0 70/18 63 50 +170
6 17.6 70/6 180/20 10 30 3/0 75/17 74 63 +135 126 114
7 16.5 95/5 230/30 5 35 5/0 80/13 67 50 + 90 120 114
8 15.1 92/8 230/35 9 40 1/0 65/15 78 66 +110 102 102
9+ 20.5 75/10 115/30 8 40 1/0 5/0 68 45 118 108
10+ 16.7 80/6 200/30 7 40 2/0 2/0 84 65 + 90
11+ 15.3 110/5 225/30 5 47 5/0 10/0 102 70 + 40 108 108
12+ 15.5 85/3 225/12 3 16 5/0 5/0 110 66 84 78
Leftheart 200/22 80/2 33 5 5/0 7/0 90 115 111 111
pressureonly 13+ 19.5 80/5 240/35 5 35 10/0 10/0 112 90 +120
altered 240/35 55/5 35 3 10/0 10/0 90 97 105 120
14=F 12.2 57/3 175/2 5 7- 135 105
15F 16.2 65/0 177/4 0 4 89 75
16=F 15.6 75/0 170/3 0 0 93 78
17F 15.4 80/0 175/3 2 6 20/3 22/3 113 75 +170 120 120
5 85/11 95/13 9 11 1/0 60/11 67 63 132 120
Rightheart 6 105/6 110/0 8 8 1/0 73/14 65 62 132 144
pressure only 11 137/12 137/10 12 11 1/0 55/8 88 88 120 116
altered 12 80/2 75/5 5 5 7/0 85/15 112 107 99 111
13 100/9 100/8 9 9 10/5 65/11 102 99 132 126
*LV =left ventricular pressure; LA =mean left atrial pressure; RV = right ventricular pressure; Ao = mean
aortic pressure; HR = Heart rate inbeats per minute. Columns A represent observations during the control period;
Brepresent the observations madefollowingalteration ofintracardiac pressure. A B.V. = thechange in systemic vascu-larvolume;AS.F. =thechangeinsystemic flow; + = carotid and aortic receptors denervated; F =carotid receptors only denervated.
HEMODYNAMIC INFLUENCES OF INTRACARDIAC BARORECEPTORS
:I
Se.i, Rot.
FIG. 1. SCHEMATIC REPRESENTATION OF THE
EXTRA-CORPOREAL CIRCUIT EMPLOYED. Blood drains by gravity
from the superior vena cava (SVC) and the inferior vena cava (IVC) into the oxygenator. The aorta (Ao.)
is cross-clamped above the coronary arteries. The level
of blood in the oxygenator is sensed by the detecting
electrodes (Det.) and blood is added to or withdrawn
from the calibrated reservoir (Res.) at the lower right-hand corner. Oxygenated blood is pumped through a
rotameter (Rot.) into the femoral artery (FA). Inter-mittently,aclamp onthe fillingline (Fill. line) isopened to permit replenishmentof the top reservoir (Res.) with
oxygenated blood.
also removed by stripping the adventitia from the
an-terior surface of the aorta between the brachiocephalic
and subclavian arteries (Table I).
At the conclusion of 6 experiments, the line through
which blood entered the left atrium from the reservoir
was occluded, resulting in anoxic cardiac arrest or
ven-tricular fibrillation. Alterations in arterial pressure were
recorded continuously for several minutes thereafter,
while systemic perfusion rate was maintained constant.
RESULTS
I. Alterations in systemic blood volume. In
all ten of the dogs in which blood volume altera-tions were measured (Table I), elevation of
in-tracardiac pressures resulted in a decline in the
extracorporeal volume and, therefore, an
augmen-tation of intravascular blood volume,whichranged from 40 to 170 ml and averaged 120 ml. A trac-ing from an experiment ofthis type is reproduced in Figure 2. In six of these animals (Dogs 1, 4-8), the pressures in the right side of the heart, the leftatrium and the left ventriclewereelevated,
and in four (Dogs 10, 11, 13, 17), the pressure
elevationwas confined to the left sideof the heart,
while right heart pressures were not altered.
The increments of intravascular volume observed in these two groups of experiments were similar.
The changes in blood volume persisted for the
en-tireperiod that the intracardiac pressureremained elevated, which in some experiments was up to
15 minutes.
II. Alterations in venous return. In Dogs 1, 3 and 4 the pressures inboth the right and left sides
of the heart were elevated. In order to maintain the extracorporeal, and therefore the intravascu-lar, blood volume constant. it was necessary to
diminish the output of thepump by 590, 540, and
220 ml per minute; this represented an average
decrease of 25.3 per cent from the control
sys-temic perfusion rates. When intracardiac pres-sures were lowered to their previous levels, ve-nous return increased but did not return to the
control levels (Figure3, Table I).
III. Alterations in systemic vascular resistance.
In Dogs
1-8,
left ventricular pressure wasele-vated from average values of 78/5 to 216/21 mm
Hg; mean left atrial pressure rose from an aver-age of 7 to an average of 25 cm H2O, and right ventricular pressure rose from average values of 6/1 to69/15 mm Hg. These pressure alterations resultedin adeclineinsystemic vascular resistance whichwas maximal approximately 1 minute later.
These maximal changes in systemic vascular
re-sistance ranged from 10 to 39 per cent and
aver-aged 24 per cent of the control resistance levels. Subsequently, the arterial pressure returned
par-tially toward control levels (Figures 2 and 4). This return was less prominent in those dogs which had undergone sinoaortic denervation.
In five experiments (Dogs 9-13) right
ven-tricular pressure was maintained constant at a low level (Table I), while left ventricular pres-sure was elevated from average values of 86/6 to
203/26 mm Hg, and mean left atrial pressure rose from an average of6 to an average of 36 cm
HO. This again resulted in a declineinsystemic vascular resistance which ranged from 20 to 40
per cent and averaged 30 per cent of the control resistance levels.
In four experiments (Dogs 14-17) left ven-tricular systolic pressure alone was elevated.
Pressure in this chamber rose from average val-ues of 69/1 to 175/3 mm Hg, while left atrial
JOHN ROSS, JR., CHARLES J. FRAHM AND EUGENE BRAUNWALD
A.
ml.
150-
100-50
-0
B.
A BLOOD VOLUME
4
; .
wl~
I
Control 0 5 10
Minutes
FIG. 2. DOG 6. A. RECORDINGS, FROM ABOVE DOWNWARD, OF PRESSURE IN THE AORTA (Ao.),
SYSTEMIC FLOW (S.F.), PRESSURES IN THE LEFT VENTRICLE (LV) AND RIGHT VENTRICLE (RV). Inthe panelon the left,left ventricular pressure was elevated. Six minutes later, in the center
panel, rightventricular pressure was alsoelevated. In the panelon theright, ventricular pres-sures were lowered.
B. THE ALTERATIONS IN SYSTEMIC VASCULAR VOLUME WHICH OCCURRED SIMULTANEOUSLY ARE
DEPICTED. The vertical arrows indicate the points in time at which left and then right ventric-ular pressures were elevated.
pressure remained low and changed little or not at all. In all of these dogs the right ventricle was decompressed with a large drainage cannula, and
intheone dog in which right ventricular pressure was measured, it did not rise. These elevations
in left ventricular systolic pressure alone resulted
in a decline in systemic vascular resistance which
ranged from 16 to 38 per cent (average, 23) of
the control resistance levels (Figure 4). In two
other experiments when left ventricular systolic
pressure was elevated from levels below 70 mm
Hg to systolic pressures of 131 and 150mm Hg, systemic vascular resistance declined 9.6 and 11.8per cent.
-LO--I -9 0. W
HENMODYNAMIC INFLUENCES OF INTRACARDIAC BARORECEPTORS
In the entire series of experiments it was ob-served that the occurrence of ventricular
extra-systoles
wNas accompanied by a brief but strikingdecline in systemic vascular resistance (Figures
3 and 5A).
I'. Alterations in heiart rate. The effects of the elevations in intracardiac pressures on heart rate were variable and slight (Table I). In
seven
experiments
the rate declined by more than 5 beats per minute; in five experiments it rose byL.A. cm.H20
10-
O-Ao.
mm.Hg.
Mrw'0.
50
0
mm.Hg
200-FIG. 3. DOG 1. THE EFFECTS OF ELEVATIONS OF PRES-SURES IN THE RIGHT VENTRICLE (RV), LEFT ATRIUM
(LA) AND LEFT VENTRICLE (LV), ACCOMPANIED BY EX-TRASYSTOLES, ON TOTAL VENOUS RETURN, AS MEASURED BY ALTERING SYSTEMIC PERFUSION RATE (S.F.). The latter
declined after intracardiac pressures were elevated and returned toward the control levels following the
reduc-tion of these pressures.
In five experiments (Dogs 5, 6, 11-13) right ventricular pressure was elevated from average
values of 4/1 to 68/12 mm Hg, while left atrial
and left ventricular pressures were maintained at
relatively constant levels. Peripheral resistance declined by only 0 to 5 per cent, with an average
fall of 3 per cent from control levels (Figure 5).
S.F ml./min.
1000
500-.
LV
mm.
H,9.
150-
-100-
_
50!
0
1
1
FIG. 4. DOG 17. ALTERATIONS IN AORTIC PRESSURE
(Ao.) AT A CONSTANT SYSTEMIC FLOW (S.F.) FOLLOWING
ELEVATION OF LEFT VENTRICULAR (LV) SYSTOLIC
PRES-SURE, ACCOMIPANIED BY A MINIMIAL ELEVATION OF LEFT
VENTRICULAR DIASTOLIC AND NIEAN LEFT ATRIAL (LA)
PRESSURE.
R.V mm.Hg.
75
-
50-
25-0
L.A.
cm.H20[
20-o-,
Ao. mm.Hg.1
50
-0
S. F
ml./min.
2000-I
JOHN ROSS, JR., CHARLES J. FRAHM AND EUGENE BRAUNWALD
i.H9.~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
...
DO-Wi
....,-50 i
FIG. 5. DOG 6. A. MINIMAL ALERATIONS IN AORTIC PRESSURE ACCOMPANYING ELEVATION OF RIGHT VENTRICULAR
PRESSURES. A more marked decline occurs near the end of thetracing following a series of extrasystoles.
B. THE EFFECT OF ALTERNATELY ELEVATING RIGHT VENTRICULAR (RV) AND LEFT VENTRICULAR (LV) PRESSURES ON
AORTIC PRESSURE (Ao.) ARE CONTRASTED. Little change results fromgradually elevating RV pressure, but a striking fall occurs when LV pressure is increased.
more than 5 beats per minute; in six it changed less than 5 beats per minute; and in two the
changes were inconsistent. The specific
cham-bers in which pressures were elevated did not ap-pear to influence these results.
V.
Effects
of cessationof flow
to the heart. In six experiments, when the inflow of blood to theheart was suddenly
terminated,
left ventricularTABLE II
Hemodynamic effects ofcessationofflow
tothe heart*
LV press. LA press. Aopress.
Dog Increase
no. A B A B A B Ao press.
mmHg cmH20 mmHg %
1 85/6 6/0 8 6 65 98 51
5 75/9 1/0 8.5 0 70 82 17
6 83/7 1/0 10 6.5 64 73 14
8 87/6 8/5 10 7 88 113 28
11 83/7 1/0 10 6.5 94 105 12
13 75/7 0/0 7.5 3.5 90 115 29
*ColumnsA representobservations madejustpriortocessationof
flowtothe heart. ColumnsB representobservations made following stabilization ofall pressures several minutesfollowingcessationof flow.
pressure declined abruptly from an average value of 81/7 mm Hg, and reached levels of less than 8/5 mm Hg within several minutes after cessa-tion of the heart beat. Right ventricular systolic pressure was less than 9 mm Hg prior to the ces-sation of perfusion and showed no significant change (Table II). In each dog systemic vas-cular resistance increased immediately, continued
torise for approximately 5 minutes and stabilized thereafter (Figure 6). These increases in sys-temic vascular resistance ranged from 14 to 51 per
centand averaged 25 per centofthe control values.
DISCUSSION
HEMODYNAMIC INFLUENCES OF INTRACARDIAC BARORECEPTORS
L.A.
cm.H20
20-
1
0-Ao.
50
50
100
Ln___..V
CESSATIONHOF9CARDIAC
:L 4-
=-FI._-_-DO 8_.EFET ON AORTI PRESSUR (Ao....
_-l-DECLINE IN INTRACARDIAC PRESSURE. Cardiac perfusion.
was stopped at the instant that the left ventricular and
left atrial pressures began to fall. An immediate
ele-vation of aortic pressure is evident.
the preparation, these interventions were found necessary to investigate the nature of the
periph-eral circulatory changes following alteration of intracardiac pressures.
.It was observed that a substantial decline in
venous returnresulted when pressures in the right
and left ventricles were elevated. The significance
of these changes in venous return is indicated by
the large changes in the output of the
extracor-poreal pump which were necessary to obviate any
alterations in intravascular blood volume. These
changes in pump output provide a measurement
of the decrease in cardiac output that would have occurred had the heart responded passively to the reflex changeinvenous return. Inaddition, when
systemic perfusion was maintained constant,
ele-vation of left heart pressures alone, or of both
left and right heart pressures, resulted in an
ex-pansion of the intravascular blood volume.
In-creases in blood volume have also been recently reported by Salisbury, Cross, and Rieben
follow-ing distention of the left ventricle with a balloon (8). Klussman, Van Citters and Rushmer, on
the other hand, did not demonstrate any changes in limb circumference or liver diameter when suction devices were applied to portions of the cardiac walls (17).
The changes in venous return and systemic blood volume following elevations of intracardiac pressures reported herein resemble those thatwere
observed when pressure withinthe isolated carotid
sinuses were elevated or when the vasodilating drug, Arfonad, was administered (12). It was previously suggested that these alterations in ve-nous return and systemic blood volume are most
likely due to dilatation of the systemic venous bed (12), because of 1) the large magnitude of the alterations in systemic vascular volume which oc-curred, and2) the fact that only 15 ml per kg of blood is estimated to be contained in the arterial and arteriolar vascular beds of the dog (18). Furthermore, arterial pressure varied inversely with total systemic blood volume, and it is there-fore possible that thechanges in the volume of the prearteriolar bed were actually opposite in direc-tion to the alteradirec-tions in total systemic blood volume. From the data presented above, it also
appears likely that an inhibition of venous tone
resulted from stimulation of the intracardiac
baroreceptors. Since splenic volume is known to
vary with alterations in sympathetic tone (19), it is of interest that the changes in blood volume resulting from elevating intracardiac pressures
were also observed in the dogs that had been
splenectomizedpreviously.
Reflexes originating from the left side of the
heart were first clearly demonstrated by Aviado and Schmidt (5). In the present experiments, when left ventricular systolic pressure was ele-vated but only minimal change in left ventricular
diastolic and left atrial mean pressures occurred, systemic vascular resistance declined. These ob-servations suggest the presence of left ventricu-lar baroreceptors sensitive to changes in systolic pressure. Indeed, bursts ofimpulses during early systole have been recorded from cardiac afferent nerve fibers by several investigators (1, 2). However, since some enlargement of the left
JOHN ROSS, JR., CHARLES J. FRAHM AND EUGENE BRAUNWALD
of left atrial pressure, the stimulation of left atrial receptors responsive to volume changes (20) can-not be completely excluded except in that ex-periment (Dog 16) in which isolated left ven-tricular perfusion resulted in absolutely no change in left atrial pressure. More striking alterations in vascular resistance were induced when left ventricular diastolic and left atrial pressures were
elevated above 10mm Hg (Figure 7). Since the hilaof the lungs were ligated in all of the experi-ments carried out on Dog 2, the large pulmonary veinsweredistended together with the left atrium. Previous studies have suggested that the pulmo-nary veins (4, 10, 11, 21 ), as well as the left atrium (7, 20) contain baroreceptor endings, and it is likely that receptors in both of these areas
participated in the observed reflexes.
Contrary to the observations of others (4, 11), only minimal declines in vascular resistance
oc-curredwhen,in the absence ofextrasystoles
(Fig-ure 5), pressures in the right side of the heart
alone were elevated. However, in the present
ex-periments, ligation of the hila prevented pressure elevation in the smaller pulmonary vessels, which perhaps contain receptors responsible for the de-cline in peripheral resistance observed by others when right heart pressures were elevated (11). In addition, in the present studies, right ventricu-lar diastolic and atrial pressures were only moder-ately elevated and provided a less extreme stimu-lus than that utilized in previous investigations (4). Accordingly, it is suggested from the pres-ent experiments that the intracardiac receptors of greatest importance in the control of systemic vascular resistance are those sensitive to elevation of left ventricular diastolic pressure and/or left atrial pressure. It is possible that the ultimate stimulus for these receptors is the stretch that occurs when the volume of the cardiac chambers is increased. However, the possibility that baro-receptors in the coronary vessels are also of
im-portance has not been excluded, since elevation
* I I. * *-- E ,1-...' 1,, a__ 1.__ n__L.vL_I... ... :
FIG. 7. DOG 2. TRACING SHOWING THE EFFECTS ON AORTIC PRESSURE OF STEP-WISE ELEVATION OF INTRACARDIAC
PRESSURES. The most profounddecline of aortic pressure occurred following elevation of mean left atrial (LA)
HEMODYNAMIC INFLUENCES OF INTRACARDIAC BARORECEPTORS
of left ventricular systolic pressure simultaneously raised the pressure in the coronary system.
It was observed that systemic vascular resist-ance fell when left ventricular systolic pressure was elevated in the range below the normal systolic blood pressure for the dog. This suggests that the left-sided intracardiac baroreceptors possess a low pressure threshold and, therefore, that these re-ceptors may be continuously activated at normal intracardiac pressures. This possibility receives support from experiments in which rhythmic im-pulses, synchronous with both ventricular and atrial contractions, were recorded from cardiac af-ferent fibers (1, 2, 9). Furthermore, the initial rapid rise in arterial pressure (Figure 6) which occurred following cessation of cardiac perfusion suggests that a continuous inhibitory influence on vascular resistance originating from the heart had beenremoved; this observation provides additional evidence for tonic activity of the intracardiac
re-ceptors. The continued and progressive elevation in arterial pressure, following cessation of cardiac perfusion, however, may have resulted from
stimulation by anoxia of receptors in the myo-cardium or coronary arteries.
In interpreting the action of reflexes originating from intracardiac receptors, the important effects of extrasystoles must be emphasized. It was ob-served in the course of these experiments that whenever extrasystoles occurred, whether during right- or left-sided pressure elevation, a striking decline in vascular resistance took place. This finding suggests that the intracardiac receptors, like those in the carotid sinus (22), are activated by rapid fluctuations in stimulation, regardless of the mean level of the stimulus applied. The oc-currence of extrasystoles during elevations in right heart pressure thus make interpretation of subsequent reflex changes difficult, and may help
to explain the results obtained by some previous investigators (4, 11).
The reflex effects of the intracardiac
barorecep-tors may be of importance in a variety of
physio-logic andpathologiccircumstances. It wouldseem
likely that they operate in conjunction with the sinoaortic mechanism in theregulation ofboth
ar-teriolar and venous tone and therefore of arterial pressure and cardiac output. In addition, when intracardiac pressures aloneare elevated, as in the presence of congestive heart failure or valvular
stenosis, the resulting arteriolar and venous dilata-tion could serve to decrease the hemodynamic burden imposed on the heart both by diminishing systemic pressure and by decreasing venous return.
SUM MARY
The effects of alterations of intracardiac pres-sures on total venous return, system vascular vol-ume and peripheral vascular resistance were stud-ied in an experimental canine preparation. The systemic vascular bed was perfused, using an ex-tracorporeal circulation, while pressures were in-dependently varied in the innervated, but hemo-dynamically isolated heart.
Elevation of intracardiac pressure (either in all four chambers or only in the left side of the heart) in ten dogs resulted in an augmentation of systemic vascular volume which averaged 120 ml.
Inthe three dogs in which the venous return was
measured, it declined by an average of 25 per
cent fromthe control levels. Significantdecreases in systemic vascular resistance were observed when left ventricular systolic pressures were ele-vated, when left ventricular diastolic and mean left atrial pressures were also elevated, or when extrasystoles occurred. Only minimal alterations in vascular resistance were observed to accom-pany elevation ofrightheart pressures alone.
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